本文選題：胃癌 + 幽門(mén)螺旋桿菌　； 參考：《安徽醫(yī)科大學(xué)》2017年碩士論文

【摘要】：【實(shí)驗(yàn)研究背景】在全世界范圍內(nèi),胃癌發(fā)病率高,大約是癌癥總發(fā)病率的8%,是癌癥致死的主要惡性疾病之一,是常見(jiàn)的惡性腫瘤。更為重要的是,約有70%的胃癌相關(guān)的死亡病例均位于不發(fā)達(dá)國(guó)家,尤其是東亞地區(qū)。在中國(guó),肺癌、乳腺癌、胃癌、肝癌、結(jié)腸癌是男性和女性中5種最常見(jiàn)的高發(fā)腫瘤。胃癌的發(fā)生是宿主基因多態(tài)性、我們?nèi)粘ｏ嬍郴蚴俏鼰煹拳h(huán)境因素、表觀遺傳學(xué)改變等多種危險(xiǎn)因素共同作用的結(jié)果。目前,幽門(mén)螺旋桿菌長(zhǎng)期慢性感染胃粘膜上皮被認(rèn)為是導(dǎo)致胃惡性腫瘤發(fā)生的最危險(xiǎn)的因素,尤其是胃腺癌。但是幽門(mén)螺旋桿菌的致病機(jī)制并不清楚,已經(jīng)報(bào)道的幽門(mén)螺旋桿菌如何與宿主基因相互作用影響胃癌的發(fā)生發(fā)展非常少。目前仍然有許多關(guān)鍵性的問(wèn)題需要進(jìn)一步探索。最近研究表明,細(xì)胞毒素相關(guān)抗原A蛋白(CagA)和細(xì)胞空泡毒素A(VacA)是幽門(mén)螺旋桿菌當(dāng)中致病性最強(qiáng)的毒力因子,研究最為廣泛。進(jìn)入細(xì)胞內(nèi)的CagA蛋白能夠異常激活NF-κB、β-catenin等信號(hào)通路,促進(jìn)細(xì)胞增殖、促炎性細(xì)胞因子產(chǎn)生及相關(guān)miRNA的產(chǎn)生等細(xì)胞反應(yīng),參與致癌過(guò)程。雖然全世界有將近一半的人感染了幽門(mén)螺旋桿菌,卻只有3%的感染人群最終發(fā)展為胃癌。這就說(shuō)明幽門(mén)螺旋桿菌感染能否致病還依賴于與宿主基因的相互作用。表觀遺傳學(xué)包括點(diǎn)突變、剪切、復(fù)制、重組、與腫瘤相關(guān)基因的甲基化等等的改變,以及腫瘤抑癌基因的失活是從炎癥轉(zhuǎn)變?yōu)榘┌Y的重要分子機(jī)制。胃癌的發(fā)生是幽門(mén)螺旋桿菌感染與細(xì)胞內(nèi)抑癌基因之間相互作用的結(jié)果。miRNA是一類(lèi)小的,非編碼的RNAs,它通過(guò)直接與靶mRNA 3′UTR結(jié)合,負(fù)向調(diào)控與腫瘤發(fā)生相關(guān)的癌基因或者抑癌基因的m RNA水平,促進(jìn)癌癥的發(fā)展。廣泛的參與到了基因的轉(zhuǎn)錄后調(diào)控。有報(bào)道研究,miR-155是免疫反應(yīng)和炎癥反應(yīng)的關(guān)鍵調(diào)控因素。但是,miR-155在幽門(mén)螺旋桿菌感染導(dǎo)致的胃疾病當(dāng)中發(fā)揮了怎樣的功能作用并不清楚,已有的報(bào)道也有相矛盾的地方。KLF4是一個(gè)含有鋅指結(jié)構(gòu)的轉(zhuǎn)錄因子。我們前期對(duì)KLF4進(jìn)行了研究,實(shí)驗(yàn)結(jié)果顯示,過(guò)表達(dá)KLF4明顯的增加了細(xì)胞的凋亡；體內(nèi)實(shí)驗(yàn)說(shuō)明過(guò)表達(dá)KLF4抑制了胃癌增殖和侵襲,KLF4在胃癌中具有抑癌基因的作用。胃癌組織中KLF4蛋白表達(dá)較正常胃粘膜上皮明顯降低,KLF4的表達(dá)和功能作用與胃癌的發(fā)生發(fā)展關(guān)系密切。但是KLF4在胃癌中表達(dá)異常的分子機(jī)制卻不清楚。我們提出了以下假設(shè):KLF4在胃癌中表達(dá)異常是不是由于幽門(mén)螺旋桿菌感染引起的?幽門(mén)螺旋桿菌中致病性最強(qiáng)的毒力因子CagA是如何與宿主基因KLF4相互作用,導(dǎo)致KLF4在胃粘膜上皮細(xì)胞異常表達(dá)?KLF4在胃癌中表達(dá)異常是否可能由于miRNA靶向干擾KLF4表達(dá)?為了探索抑癌基因KLF4在胃癌中表達(dá)降低可能存在的分子機(jī)制,本課題在細(xì)胞水平上和臨床病例相結(jié)合的方式進(jìn)行實(shí)驗(yàn)驗(yàn)證�！緦�(shí)驗(yàn)研究方法】1、Western blot檢測(cè)胃粘膜上皮細(xì)胞和胃癌細(xì)胞中KLF4蛋白表達(dá)。將HA標(biāo)記的WT-CagA質(zhì)粒轉(zhuǎn)染進(jìn)入GES-1細(xì)胞,通過(guò)轉(zhuǎn)染不同的時(shí)間、不同的劑量,檢測(cè)GES-1細(xì)胞中KLF4蛋白和m RNA表達(dá)。2、免疫組化方法檢測(cè)胃癌組織和癌旁組織中KLF4蛋白表達(dá)。3、將HA標(biāo)記的WT-CagA質(zhì)粒轉(zhuǎn)染進(jìn)入GES-1細(xì)胞,細(xì)胞行為學(xué)實(shí)驗(yàn)檢測(cè)CagA對(duì)GES-1細(xì)胞惡性生物學(xué)行為的影響。4、搜集33例體檢者和胃癌患者血清標(biāo)本,提取血清中miRNA,用RT-PCR的方法檢測(cè)miR-155表達(dá)的差異性；原位雜交方法檢測(cè)胃癌組織和癌旁組織中miR-155表達(dá)。5、RT-PCR檢測(cè)胃粘膜上皮細(xì)胞和胃癌細(xì)胞株中miR-155的表達(dá)。將HA標(biāo)記的WT-CagA質(zhì)粒轉(zhuǎn)染進(jìn)入GES-1中,提取細(xì)胞中總RNA。用普通PCR的方法,瓊脂糖凝膠電泳觀察CagA對(duì)miR-155表達(dá)的影響。6、在GES-1細(xì)胞中瞬時(shí)轉(zhuǎn)染miR-155-3p minic和miR-155-5p-minic,普通PCR檢測(cè)其對(duì)KLF4 mRNA影響；通過(guò)轉(zhuǎn)染不同的時(shí)間、不同的劑量,Western blot檢測(cè)其對(duì)KLF4蛋白表達(dá)的影響；WT-KLF4 luciferase reporter和MUT-KLF4 luciferase reporter與miR-155 minic/NC共轉(zhuǎn)染,48h后檢測(cè)熒光素酶活性,從而對(duì)miR-155下游靶點(diǎn)的預(yù)測(cè)進(jìn)行驗(yàn)證。7、建立穩(wěn)定表達(dá)miR-155-5p-negative controlmiR-155-5p minic的胃粘膜上皮細(xì)胞株GES-1和胃癌細(xì)胞株AGS。建立穩(wěn)定表達(dá)miR-155-5p-negativemiR-155-5p-inhibitor的胃癌細(xì)胞株SGC-7901。通過(guò)western blot實(shí)驗(yàn)分析穩(wěn)定表達(dá)miR-155和敲低miR-155的細(xì)胞株中,KLF4蛋白表達(dá)�！緦�(shí)驗(yàn)研究結(jié)果】1、與正常的胃粘膜上皮細(xì)胞相比,胃癌細(xì)胞株當(dāng)中KLF4蛋白表達(dá)明顯降低；高表達(dá)CagA后很明顯的降低了KLF4蛋白和m RNA表達(dá),并且呈現(xiàn)出時(shí)間和劑量依賴性的抑制；2、免疫組化結(jié)果顯示,胃癌組織當(dāng)中KLF4的表達(dá)明顯降低,且幽門(mén)螺旋桿菌感染的胃癌組織KLF4表達(dá)降低更為明顯。3、幽門(mén)螺旋桿菌毒力因子CagA的高表達(dá)促進(jìn)了胃粘膜上皮細(xì)胞的增殖、遷移、平板克隆等惡性生物學(xué)行為的改變。4、與正常人的血清相比,胃癌患者血清標(biāo)本中miR-155的表達(dá)增高,尤其在TNM分期Ⅱ期和Ⅲ期更為明顯；并且miR-155表達(dá)的升高與幽門(mén)螺旋桿菌感染密切相關(guān)。miR-155在胃癌組織中表達(dá)明顯高于癌旁組織。5、細(xì)胞水平上,在胃上皮細(xì)胞GES-1和惡性程度相對(duì)較低的胃癌細(xì)胞株AGS表達(dá)相對(duì)較低,在惡性程度較高的胃癌細(xì)胞株中miR-155表達(dá)水平相對(duì)較高；高表達(dá)CagA誘導(dǎo)了miR-155表達(dá)上調(diào)；6、熒光素酶報(bào)告基因證實(shí)KLF4可能是miR-155的靶基因。7、成功構(gòu)建了穩(wěn)定表達(dá)miR-155-5p-negative controlmiR-155-5p minic的胃粘膜上皮細(xì)胞株GES-1和胃癌細(xì)胞株AGS。建立了穩(wěn)定表達(dá)miR-155-5p-negativemiR-155-5p-inhibitor的胃癌細(xì)胞株SGC-7901。Western blot結(jié)果顯示miR-155可能負(fù)向調(diào)控KLF4表達(dá)�！窘Y(jié)論】CagA可能通過(guò)誘導(dǎo)miR-155表達(dá),靶向干擾KLF4轉(zhuǎn)錄及翻譯,抑制KLF4表達(dá),從而促進(jìn)胃粘膜上皮的惡性轉(zhuǎn)化。
[Abstract]:[background] the incidence of gastric cancer is high around the world, about 8% of the total cancer incidence, one of the major malignant diseases fatal to cancer and a common malignant tumor. More importantly, about 70% of the cancer related deaths are in the underdeveloped countries, especially in East Asia. In China, lung cancer, and breast cancer, Gastric cancer, liver cancer, and colon cancer are the 5 most common high incidence tumors in men and women. The occurrence of gastric cancer is the result of host gene polymorphism, environmental factors such as our daily diet or smoking, epigenetic changes and other risk factors. The most dangerous factors for the occurrence of gastric malignant tumors, especially gastric adenocarcinoma. However, the pathogenesis of Helicobacter pylori is not clear. It is reported that the interaction of Helicobacter pylori and host genes affects the development of gastric cancer very little. There are still many key problems that need further exploration. Recent studies have shown that Cytotoxin related antigen A (CagA) and cell vacuolating toxin A (VacA) are the most virulent among Helicobacter pylori, the most widely studied. The CagA proteins entering the cell can activate abnormal activation of NF- kappa B, beta -catenin and other signaling pathways, promote cell proliferation, proinflammatory cytokines production and related miRNA production. Although nearly half of the world is infected with Helicobacter pylori, only 3% of the infected people eventually develop into gastric cancer. This suggests that the infection of Helicobacter pylori is also dependent on the interaction with the host gene. Epigenetics includes point mutations, shear, replication, recombination, and tumor related groups. Changes in methylation, and the inactivation of tumor suppressor genes are important molecular mechanisms from inflammation to cancer. The occurrence of gastric cancer is the result of the interaction between Helicobacter pylori infection and intracellular tumor suppressor genes.MiRNA is a small, non coded RNAs, which is regulated by a direct combination with the target mRNA 3 'UTR. M RNA levels associated with oncogenesis, or tumor suppressor genes, promote cancer development. Extensive involvement in post transcriptional regulation of genes. MiR-155 is a key regulator of the immune response and inflammatory response. However, what is the function of miR-155 in the gastric disease caused by Helicobacter pylori infection The effect is not clear, the existing reports also have a contradictory place.KLF4 is a transcriptional factor containing the zinc finger structure. We studied the KLF4 earlier. The experimental results showed that overexpression of KLF4 significantly increased the apoptosis of the cells; in vivo experiments showed that overexpression of KLF4 inhibited the proliferation and invasion of gastric cancer, and KLF4 had tumor suppressor in gastric cancer. The expression of KLF4 protein in gastric cancer tissue is significantly lower than that of normal gastric mucosa, and the expression and function of KLF4 are closely related to the development of gastric cancer. However, the molecular mechanism of abnormal expression of KLF4 in gastric cancer is not clear. We put forward the following hypothesis: the abnormal expression of KLF4 in gastric cancer is not due to the Helicobacter pylori How is the strongest virulence factor CagA in Helicobacter pylori caused by the interaction of the host gene KLF4 and the abnormal expression of KLF4 in the epithelial cells of the gastric mucosa? Is the abnormal expression of KLF4 in gastric cancer possibly due to the miRNA targeting KLF4 expression? In order to detect the reduction of the expression of the tumor suppressor gene KLF4 in gastric cancer, the possible survival of the tumor suppressor gene KLF4 may exist. In the molecular mechanism, the subject was tested in a combination of cell level and clinical case. [experimental method] 1, Western blot was used to detect the expression of KLF4 protein in gastric epithelial cells and gastric cancer cells. HA labeled WT-CagA plasmid was transfected into GES-1 cells, and different doses were detected by transfection at different time. The expression of KLF4 protein and m RNA in GES-1 cells was.2, and the expression of KLF4 protein in gastric cancer tissues and adjacent tissues was detected by immunohistochemistry. The WT-CagA plasmids labeled with HA were transfected into GES-1 cells. The effect of CagA on the malignant biological behavior of GES-1 cells was detected by cell behavior test. 33 cases of physical examination and gastric cancer patients were collected and extracted. MiRNA in serum was used to detect the difference in expression of miR-155 by RT-PCR. In situ hybridization was used to detect the expression of miR-155 in gastric cancer tissue and adjacent tissues, and the expression of miR-155 in gastric epithelial cells and gastric cancer cell lines was detected by RT-PCR. The WT-CagA plasmid labeled with HA was transfected into GES-1, and the general PCR method was extracted. The effect of CagA on the expression of miR-155 was observed by agarose gel electrophoresis,.6, miR-155-3p minic and miR-155-5p-minic were transiently transfected in GES-1 cells. Ordinary PCR detected its effect on KLF4 mRNA. Luciferase reporter was co transfected with miR-155 minic/NC, and the activity of luciferase was detected after 48h, thus the prediction of the target of the downstream target of miR-155 was verified by.7, and the stable expression of GES-1 and gastric cancer cell strain of the gastric mucosa epithelial cell line, which expressed the miR-155-5p-negative controlmiR-155-5p minic, was established. The gastric cancer cell line SGC-7901. of itor analyzed the expression of KLF4 protein in the cell lines expressing miR-155 and low miR-155 by Western blot test. [experimental results] 1, the expression of KLF4 protein in gastric carcinoma cell lines decreased significantly compared with normal gastric mucosal epithelial cells, and KLF4 protein and M decreased after high expression of CagA. The expression of RNA was expressed in time and dose dependent inhibition. 2, the results of immunohistochemistry showed that the expression of KLF4 in gastric carcinoma tissue decreased obviously, and the expression of KLF4 in gastric cancer tissues of Helicobacter pylori decreased more obviously.3. The high expression of CagA of Helicobacter pylori promoted the proliferation and migration of gastric mucosa epithelial cells. The changes in the malignant biological behavior such as the flat clones.4, compared with the normal human serum, the expression of miR-155 in the serum samples of the gastric cancer patients was increased, especially in the stage II and stage III of the TNM stage, and the expression of miR-155 was closely related to the Helicobacter pylori infection and the expression of.MiR-155 in gastric cancer tissues was significantly higher than that of the para cancerous tissue.5. On the cell level, the expression of AGS in gastric epithelial cell GES-1 and the relatively low malignancy of gastric cancer cell line was relatively low, and the expression level of miR-155 was relatively high in high malignant gastric cancer cells; high expression CagA induced the up-regulated expression of miR-155; 6, the luciferase reporter gene confirmed that KLF4 might be the target gene.7 of miR-155. The gastric mucosal epithelial cell line GES-1 and the gastric cancer cell line that stably expressed miR-155-5p-negative controlmiR-155-5p minic were constructed, and the gastric cancer cell line AGS. was established to stabilize the expression of miR-155-5p-negativemiR-155-5p-inhibitor in the gastric cancer cell line SGC-7901.Western blot results showed that miR-155 may be negatively regulated KLF4 expression. [Conclusion] CagA may be induced by lure. The expression of miR-155 can interfere with KLF4 transcription and translation, inhibit KLF4 expression, and promote malignant transformation of gastric epithelial cells.

【學(xué)位授予單位】：安徽醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類(lèi)號(hào)】：R735.2

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